The fungus Neurospora crassa is a very useful model for DNA-repair studies in eukaryotes because it is easy to maintain, to study genetically, and to handle biochemically. Using zymolyase lysis of cells on top of alkaline sucrose gradients, we have shown that the pyrimidine dimer excision-defective uvs-2 strain has a post-replication-repair system very similar to that of other eukaryotes. After ultraviolet-light irradiation, DNA synthesis is depressed and DNA is made in short segments for an abnormal length of time, due to blockage of synthesis by dimers. Eventually, the blockage is overcome and normal length DNA is made, although dimers remain in the template and DNA synthesis remains depressed. Caffeine slows, but does not block recovery. The process does not involve recombinational transfers of dimers to newly made DNA. Unlike other eukaryotes there may be gaps at the site of pyrimidine dimers before they are bypassed. We plan to examine mutagen sensitive mutants for blocks in this system and to examine replicon length and initiation patterns in Neurospora chromatin. These results validate the use of Neurospora for mutagenesis studies and should help uncover the mechanisms underlying this repair system which is thought to be fundamental in mutation and cancer induction.